Disease relevance of sulfaniumyl

• Therefore, a treatment that reduces colonic H2S levels could be clinically useful in the treatment of flatus odor and of ulcerative colitis [1].
• The third gas: H2S regulates perfusion pressure in both the isolated and perfused normal rat liver and in cirrhosis [2].
• Hydrogen sulfide (H2S), a recently discovered gas neurotransmitter, is a putative vasodilator whose role in hepatic vascular regulation and portal hypertension is unexplored [2].
• D-cysteine, a powerful inhibitor of Escherichia coli growth, is decomposed in vitro into pyruvate, H2S, and NH3 by D-cysteine desulfhydrase [3].
• Inhibition of H2S formation may therefore be a novel approach in acute stroke therapy [4].

Psychiatry related information on sulfaniumyl

• Considerably lower H2S levels are reported in the brains of Alzheimer's disease (AD) patients, where levels of brain protein nitration (probably mediated by peroxynitrite) are markedly increased [5].
• To address this further we assessed olfaction by three methods-a smell identification test ("UPSIT") in 58 patients and 135 controls; olfactory-evoked response (OEP) to H2S in 15 patients, and pathological examination of olfactory bulbs obtained from 8 cadavers [6].
• The logistic regression was analyzed for estimation of the association between an organoleptic evaluation greater than a slight level and the groups with CH3SH, H2S or total VSC with concentrations above the optimum cut-off value [7].
• We observed significant reductions in motor activity, water maze performance, and body temperature following exposure only to high concentrations (> or = 80 ppm) of H2S [8].

High impact information on sulfaniumyl

• The HNC, H2CO, H2S, and CS abundances relative to H2O measured during breakup are consistent with those obtained in other comets [9].
• CONCLUSIONS: The ability of bismuth subsalicylate to dramatically reduce H2S could provide a clinically useful means of controlling fecal and/or flatus odor and of decreasing the putative injurious effects of H2S on the colonic mucosa [1].
• Both S0 and polysulfide served as substrates for H2S production, and the S0 reduction activity but not the H2-oxidation activity was enhanced by the redox protein rubredoxin [10].
• In conclusion, CSE-derived H2S is involved in the maintenance of portal venous pressure [2].
• We also show that physiological concentrations of H2S selectively enhance NMDA receptor-mediated responses and facilitate the induction of hippocampal long-term potentiation [11].

Chemical compound and disease context of sulfaniumyl

• Although ATP synthesis in mitochondria usually involves the oxidation of reduced carbon compounds, many alpha-proteobacteria and some mitochondria are known to use sulfide (H2S) as an electron donor for the respiratory chain and its associated ATP synthesis [12].
• The effects of the Beggiatoa sp. on vertical gradients of O2, H2S, pH, and NO3- were determined with microsensors [13].
• Salmonella typhimurium produces H2S from thiosulfate or sulfite [14].
• Male Wistar rats were subjected to acute endotoxemia (Escherichia coli lipopolysaccharide (LPS) 6 mg kg(-1) intravenously (i.v.) for 6 h) and treated with vehicle (saline, 1 ml kg(-1) i.v.) or DL-propargylglycine (PAG, 10-100 mg kg(-1) i.v.), an inhibitor of the H2S-synthesizing enzyme cystathionine-gamma-lyase (CSE) [15].
• Methylmercury toxicity was counteracted by exogenously added HS-, and both met2 and met17 (met15) mutants overproduced H2S [16].

Biological context of sulfaniumyl

• In summary, these results confirm the ability of CBS to produce H2S, but show in contrast to prior reports that the major mechanism is via beta-replacement and not cysteine hydrolysis [17].
• Methemoglobin also abolished the inhibitory effect of exogenous H2S on cell proliferation [18].
• In the present study, we used CSE stably overexpressed HEK-293 cells to explore the effect of the CSE/H2S system on cell growth and proliferation [18].
• Hydrogen sulphide (H2S) has recently been identified as a novel gaseous transmitter that induces vasodilatation through activation of K(ATP) channels in vascular smooth muscle cells [19].
• H2S hyperpolarized membrane potentials by -12 mV in nystatin-perforated VSMC [20].

Anatomical context of sulfaniumyl

• In the present study, using the whole-cell and single-channel patch-clamp technique, we demonstrated that exogenous H2S activated K(ATP) channels and hyperpolarized cell membrane in rat mesenteric artery VSMC [20].
• Regulation of sulfur nutrition in wild-type and transgenic poplar over-expressing gamma-glutamylcysteine synthetase in the cytosol as affected by atmospheric H2S [21].
• These observations suggest that the increase in [Ca2+]i in response to H2S involves both calcium influx across the plasma membrane and calcium release from intracellular stores [22].
• The nucleosome core particle, containing 145 base pairs of DNA and a histone core (two each of the four histones H2S, H2B, H3, and H4), was isolated from chicken erythrocytes [23].
• Plasma hydrogen sulfide (H2S), and H2S generation by thoracic aorta and superior mesenteric artery, were determined [24].

Associations of sulfaniumyl with other chemical compounds

• CSE uses L-cysteine as a substrate to produce hydrogen sulfide (H2S) [18].
• We also show that AdoMet stimulates this H2S producing reaction but that there is no evidence for stimulation by calcium and calmodulin as reported previously [17].
• Quenching rate constants for O2 and CO are relatively insensitive to protein differences, while H2S and CS2 are somewhat more sensitive [25].
• Lowering endogenous H2S level with, D,L-propargylglycine and beta-cyano-L-alanine, two CSE inhibitors, significantly decreased [Ca2+]i, suggesting that endogenous H2S may have a positive tonic influence on [Ca2+]i homeostasis [22].
• O-Acetyl-L-serine sulfhydrylase catalyzes the final step in the biosynthesis of cysteine from H2S and O-acetyl-L-serine in the fungus Cephalosporsium acremonium, a cephalosporin C-producing organism [26].

Gene context of sulfaniumyl

• The activation of ERK by H2S in HASMCs was accompanied by increased caspase-3 activity [27].
• Reactions catalyzed by the cystathionine beta-synthase enzyme (CBS) are one possible source for the production of H2S [17].
• The toxicity of H2S has been attributed to its ability to inhibit cytochrome c oxidase in a similar manner to HCN [28].
• This discovery accelerated the identification of an H2S-producing enzyme, cystathionine beta-synthase (CBS) in the brain [29].
• Reduction of oxytocin receptors by hydrosulfide ion may be a mechanism by which low levels of H2S delay parturition in rats [30].

Analytical, diagnostic and therapeutic context of sulfaniumyl

• We expressed and purified corresponding peptides, H1S and H2S, and confirmed by circular dichroism spectroscopy that they can assume alpha-helical conformation [31].
• Using RT-PCR, only cystathionine gamma-lyase (CSE), a H2S producing enzyme, was detected in primary cultures of microglia [22].
• In contrast, castration of male mice decreases the levels of testosterone, SAM and H2S in the brain [32].
• Gradients of O2, H2S, and pH were examined with microelectrodes during incubation [33].
• In conclusion, our findings provide the first evidence that H2S may protect the heart most probably by activating sarcolemmal KATP channels and/or provoking NO release and the cardioprotective effects of metabolic ischemic preconditioning is, at least partially, mediated by endogenous H2S [34].

References